Fatality, atropine causing

Certain mushrooms, especially those of the genus Inocybe, contain muscarinic alkaloids. Ingestion of these mushrooms causes typical signs of muscarinic excess within 15-30 minutes. These effects can be very uncomfortable but are rarely fatal. Treatment is with atropine, 1-2 mg parenterally. (Amanita muscaria, the first source of muscarine, contains very low concentrations of the alkaloid.)... 

Fatalities from intoxication with atropine and scopolamine are rare, but they sometimes occur in children, in whom 10 mg or less may be lethal. Idiosyncratic reactions are more common with scopolamine chan with atropine, and ordinary therapeutic doses sometimes cause alarming effects. Table 1 lists undesirable responses or symptoms of overdose associated with various doses of atropine. 

TTie ability of certain drugs to cross the ocular and nasolacrimal epithelium means that these drugs are to some extent absorbed systemically. The degree to which this occurs in the horse has not been investigated extensively. However, topical atropine has been recognized as causing transient ileus, particularly in foals, and has been implicated in a very small number of fatal colic cases in adult horses (Brooks 1999). Dexametha-sone has been detected in the serum of horses 24 h after cessation of administration of a 0.1% ointment three times a day (Speiss et al 1999) and trainers of competition horses should be made aware of the possibility of forensic detection of topically administered ophthalmic drugs. 

In cases of attempted suicide, often fatal intoxications occur where, in spite of early hospitalization, patients are beyond remedy. Initially, signs of recovery may be observed, but after 2-3 days patients relapse with a measurable increase in OP plasma concentrations. This phenomenon is called intermediary syndrome (IMS), first described by Senananyake et al. in 1987, and is possibly a consequence of a severe intoxication with permanent depolarization of the neuromuscular end-plates and constant excitation of the nicotinic acetylcholine receptors in the CNS of the patient. The IMS is clinically characterized by acute respiratory paresis, weakness of facial, palatal, external ocular, nuchal and proximal limb muscles and depressed tendon reflexes. Some authors propose that an insufficient therapy with oximes or atropine (see Section 9.2.5) and inadequate artificial respiration in the early stages of intoxication may cause the occurrence of an IMS. It is further remarkable that only some distinct OP agents (e.g. fenthion, dimethoate, monocrotophos and methamidophos) seem capable of producing the IMS. 

The inhibition of AChE leads to the accumulation of the neurotransmitter ACh in synapses of the central and peripheral nervous systems and over-stimulation of post-synaptic cholinergic receptors. Exposure to even small amounts of an organophosphorus compound can be fatal as the poison causes seizures, convulsions and lesions of the central nervous system. The current standard treatment for poisoning usually consists of combined administration of anticholinergic drugs (preferably atropine) and AChE reactivators (called oximes). 

Well-known symptoms of sarin toxicity include miosis, hypersecretions, bradycardia, and fasciculations. However, the mechanism of organophosphate toxicity seems to involve conflicting actions. For example, mydriasis or miosis, and bradycardia or tachycardia may occur. Acute respiratory insufficiency is the most important cause of immediate death. Early symptoms include (i) tachypnea due to increased airway secretions and bronchospasm (a muscarinic effect), (ii) peripheral respiratory muscle paralysis (a nicotinic effect), and (iii) inhibition of respiratory centers (a CNS effect), all of which lead to severe respiratory deficiency. If left untreated at this stage, death will result. Cardiovascular symptoms may include hypertension or hypotension. Various arrhythmias can also occur, and caution is required when the QT interval is prolonged. In particular, if hypoxemia is present, fatal arrhythmias may occur with intravenous administration of atropine... 

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